Background Tumor growth can be addicted to vital oncogenes, but whether long noncoding RNAs (lncRNAs) are essential to cancer survival is largely uncharacterized. Methods We retrieved Gene Expression Omnibus datasets to identify lncRNA overexpression in 257 cancers vs 196 normal tissues and analyzed the association of ST8SIA6-AS1 (termed Aurora A/Polo-like-kinase 1 [PLK1]–associated lncRNA, APAL) with the clinical outcomes of multiple types of cancer from public RNA sequencing and microarray datasets as well as from in-house cancer cohorts. Loss- and gain-of-function experiments were performed to explore the role of APAL in cancers in vitro and in vivo. RNA pulldown and RNA immunoprecipitation were used to investigate APAL-interacting proteins. All statistical tests were two-sided. Results APAL is overexpressed in multiple human cancers associated with poor clinical outcome of patients. APAL knockdown causes mitotic catastrophe and massive apoptosis in human breast, lung, and pancreatic cancer cells. Overexpressing APAL accelerates cancer cell cycle progression, promotes proliferation, and inhibits chemotherapy-induced apoptosis. Mechanism studies show that APAL links up PLK1 and Aurora A to enhance Aurora A-mediated PLK1 phosphorylation. Notably, targeting APAL inhibits the growth of breast and lung cancer xenografts in vivo (MCF-7 xenografts: mean tumor weight, control = 0.18 g [SD = 0.03] vs APAL locked nucleic acids = 0.07 g [SD = 0.02], P < .001, n = 8 mice per group; A549 xenografts: mean tumor weight control = 0.36 g [SD = 0.10] vs APAL locked nucleic acids = 0.10 g [SD = 0.04], P < .001, n = 9 mice per group) and the survival of patient-derived breast cancer organoids in three-dimensional cultures. Conclusions Our data highlight the essential role of lncRNA in cancer cell survival and the potential of APAL as an attractive therapeutic target for a broad-spectrum of cancers.

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Due to the competitive growth on the crystal face of seed, it is always difficult to control the morphology of the formation of nanoparticles precisely by a seed-mediated growth method.

Contrast to the polydisperse nanorods formed by common seed-mediated growth method without the presence of cetyltrimethylammonium bromide (CTAB) in seed solution, we successfully obtained silver nanoparticles with different morphologies in the same reaction system by addition of CTAB in the seed solution. In this work, an appropriate amount of CTAB was added into the solution to prepare silver seed crystals. The results show that the aging time of silver seeds have a great influence on the sizes and morphologies of silver nanoparticles and thus the shape-controllable silver nanoparticles can be easily achieved by simply changing the seed aging time. The results also support that the selective adsorption ability or adsorption behavior of TSC can be adjusted by adding CTAB in the preparation procedure of silver seeds. We suggest that different aging times generate different effects on the competitive adsorption between CTAB and citrate to induce the orientation growth of silver seeds. As a result, silver nanospheres, nanorods, and triangular nanoplates can be easily prepared in the same system. In addition, we overcome the time limitation about the use of the seeds by adding CTAB into seed solution and make the synthesis of silver or other metal nanoparticles with different morphologies more easily and more efficiently. Electronic supplementary material The online version of this article (10.1186/s11671-019-2898-x) contains supplementary material, which is available to authorized users.